Endothelial Cell Senescence Increases Traction Forces due to Age-Associated Changes in the Glycocalyx and SIRT1

Cheung, Tracy M.; Yan, Jessica B.; Fu, Justin J.; Huang, Jianyong; Yuan, Fan; Truskey, George A.

doi:10.1007/s12195-014-0371-6

Cited by 20 publications

(18 citation statements)

References 67 publications

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“…Ageing occurs as a result of cellular senescence, and the occurrence and development of age-related cardiovascular diseases are associated with the senescence of vascular cells (Cheung et al, 2015). Cell senescence is a complex pathophysiological process, which involves multiple factors regulated by the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Li¹,

Yan²,

Zhang³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The development of age-related cardiovascular disease is associated with the senescence of vascular cells. This study aimed to investigate the effect of ginsenoside Rg1 on vascular smooth muscle cell (VSMC) senescence. Primary VSMCs were cultured and divided into control, D-galactose (D-gal), Rg1-L, and Rg1-H groups, which were cultured without and with D-gal, and with low-and highconcentrations of Rg1, respectively. D-gal-induced cellular senescence was identified by b-galactosidase staining, and ultrastructural changes within the cells were observed. The expression of p16, p21, and p53 in the four groups of VSMCs was determined by western blotting, and the cell cycle was investigated by flow cytometry. Compared with the control group, there was an obvious change in the ultrastructure of VSMCs in the D-gal group, and the proportion of b-galactosidasepositive cells was significantly increased (P < 0.05). In addition, p16, p21, and p53 expression was significantly increased (P < 0.05) and the cell cycle was arrested in the G0/G1 phase. Compared with the D-gal group, the percentage of positive cells was significantly reduced (P < 0.05) in the Rg1 groups, the expression of p16, p21, and p53 was significantly reduced (P < 0.05), and the number of cells in the G0/G1 phase decreased (P < 0.05). Ginsenoside Rg1 can inhibit VSMC senescence, and the mechanisms may be related to its partial inhibition of the p16 INK4a /Rb and p53-p21Cip1/Waf1 signaling pathways during the cell cycle.

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Section: Introductionmentioning

confidence: 99%

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Li¹,

Yan²,

Zhang³

et al. 2016

Genet. Mol. Res.

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“…During senescence the glycocalyx of vascular endothelium and erythrocytes is gradually compromised [45, 46]. In dialysis patients this process is supposedly accelerated.…”

Section: Discussionmentioning

confidence: 99%

Erythrocyte Sodium Sensitivity and Eryptosis in Chronic Hemodialysis Patients

Meyring-Wösten

Kuntsevich

Campos

et al. 2017

Kidney Blood Press Res

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Background/Aims: In hemodialysis (HD) patients the endothelial and erythrocyte glycocalyx is impaired which in turn correlates with elevated erythrocyte sodium sensitivity (ESS). Additionally, apoptotic erythrocyte death (eryptosis), characterized by phosphatidylserine (PS) exposure on the cell surface, is increased in this population. We aimed to explore the relationship of ESS and eryptosis. Methods: Blood samples were collected from 11 healthy controls and 20 chronic HD patients before and after midweek HD. ESS was quantified by the salt blood test. PS-exposure, intracellular reactive oxygen species (ROS) of erythrocytes and reticulocytes were assessed by flow cytometry. Results: Compared to controls ESS was significantly higher in HD patients preHD and did not change during treatment. The percentage of eryptotic cells did not differ between controls and patients preHD. However, eryptosis decreased during HD. ESS and eryptosis were uncorrelated, while eryptosis was positively correlated with intracellular ROS and percent reticulocytes. Conclusions: Higher ESS levels in HD patients indicate a pathologic glycocalyx. ESS and eryptosis were not correlated. The decreased eryptosis postHD may possibly be related to dialytic uremic toxin removal, but is likely multifactorial. The relationship between eryptosis and intracellular ROS warrants further research.

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“…Filamentous actin (F-actin) is critical for stress responses and also mediates ECM nuclear–mechanical coupling [ 37 ]. Cheung et al investigated whether the senescence of human endothelial cells (ECs) is associated with an increase in traction forces through modification in the antioxidant regulator deacetylase Sirtuin1 (SIRT-1), commonly downregulated during aging [ 38 ]. The authors found that traction forces were higher in aged ECs, and this increase correlated with abnormal actin localization.…”

Section: Mechanical Changes In Aging Cytoskeletonmentioning

confidence: 99%

Stiffness and Aging in Cardiovascular Diseases: The Dangerous Relationship between Force and Senescence

Ferrari

Pesce

2021

IJMS

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Biological aging is a process associated with a gradual decline in tissues’ homeostasis based on the progressive inability of the cells to self-renew. Cellular senescence is one of the hallmarks of the aging process, characterized by an irreversible cell cycle arrest due to reactive oxygen species (ROS) production, telomeres shortening, chronic inflammatory activation, and chromatin modifications. In this review, we will describe the effects of senescence on tissue structure, extracellular matrix (ECM) organization, and nucleus architecture, and see how these changes affect (are affected by) mechano-transduction. In our view, this is essential for a deeper understanding of the progressive pathological evolution of the cardiovascular system and its relationship with the detrimental effects of risk factors, known to act at an epigenetic level.

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Endothelial Cell Senescence Increases Traction Forces due to Age-Associated Changes in the Glycocalyx and SIRT1

Cited by 20 publications

References 67 publications

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Erythrocyte Sodium Sensitivity and Eryptosis in Chronic Hemodialysis Patients

Stiffness and Aging in Cardiovascular Diseases: The Dangerous Relationship between Force and Senescence

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